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@niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists
A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient).
there is no washout period and the order of drugs given isn't switched
Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please?
hi, but inferior oblique moves up and in and not out
and why no therapy, i.e. cognitive training`
Amazing video dude. Somehow never learned this in neuro lol.
"live-born offspring" ← baited
why is it 50% females tho?
felt like an idiot after i figured out why i got this wrong.
This question makes me want to vomit
That's a modern day mystery.
The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend.
aka 'merica #firstworldproblems
I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps!
the only reason I got this right was because they described the tumour as being near the falx cerebri.
Other hints include being described as round and seen in a female. Both indicative of Meningioma
also meningiomas typically present with seizures or focal neurological signs
you're definitely not alone lol
And its not in FA, so fuck it IMO
I guessed it because the names sounded similar :D
I also guessed because both words start with "glu")))
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
Not a clue. This was so random.
This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around)
I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps!
Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea
Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected.
Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)?
we had the exact same thought process, so i too am hoping this is the correct way to approach it
get reasoning friend
the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_-
Also misread the question, thought about the lab volumes of the BLOOD smh
yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH
missed this question for the same reason .. still pissed
This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral).
Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness.
I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function.
Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative?
Great explanation guys
this is disgusting.
How is that NOT posterior to middle concha? bad question
@yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw)
Sphenoethmoidal RECESS not sphenoethmoidal SINUS
yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons.
I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic?
The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms.
More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico).
Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities.
I'm shocked that I found a fellow puerto rican on this site! Good luck on your test!
dont be shocked! me too! exito!
I was thinking that its Murine typhus transmitted by fleas
Im mad at how simple this question actually is
Incidence is measured from those AT RISK. People with the disease are not considered to be at risk. So 2500 - 500 = 2000 people at-risk. Of those 2000, within one year 200 develop the disease. So 200/2000 of the at-risk population develop the disease. 20/2000 = 10% = incidence
The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering:
chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities
Turner syndrome patients are also chromatin negative as well though....
I didn't know a complication post-meningitis was lack of humor.
Ah, didn't read the last line. Yeah, that is taking it a bit far
yall are haters. this is the first explanation that has ever made sense to me
https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased...
How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA?
According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative.
This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive."
i really hate haters this is awesome!
No sertoli cells or lack of mullerian inhibitory factor makes more sense. bc there is both male and female internal genitalia but only male external genatalia. and karyotype would show 46XY. First Aid 2018 pg. 604 - the "Sexual Differentiation" charge delineates exactly this. If it were 5areductase deficiency the child would have testicles and scrotum, which in this case is absence. Hope this makes sense. Please let me know if you disagree and why. Thanks.
I believe the tricky part is that they don't mention the status of the Male external genitalia. Pg. 605 from FA ( bottom portion) shows the external development of the Male/Female genitalia; you see DHT is need for male. Furthermore, pg. 604 (SEXUAL DIFFERENTIATION) DHT is also needed for Male external development.
My understanding of this is that the diagnosis is 5alpha reductase deficiency because the newborn has female external (aka ambiguous) with male internal (aka "male genital ducts"). According to FA, leydig cells produce testosterone, which can either stimulate the mesonephric duct to form the INTERNAL male genitals (as see in the pt). Testosterone can also be acted on by 5alpha reductase to become Dihydrotestosterone, which forms the male EXTERNAL genitalia. Since this kid has "female" genitals, but has male insides and is 46XY, id say this is a simple case of 5alpha reductase deficiency.
No sertoli cells or no MIF would present as both female and male internal (because MIF typically inhibits differentiation of female internal) and male external genitalia (bcuz leydig cells are unaffected)
yea, aeresol transmission via bat poop in caves
Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me.
But tyrosine can come from phenylalanine, so it's not really essential right?
in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected.
Note: Tyrosine is ONLY essential with PKU in children
bro FA2018 lists tyrosine as an essential AA. They played us.
Thank you for your explanation!
One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated?
I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes.
I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question.
According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up?
rhinorrhea is specific to withdrawal from opioids (aka heroin). Look at page 554 in FA2018
what if the alcoholic just has a concurrent rhinovirus infection ;)
what would his diagnosis be tho?
@niboonsh Giardia I believe. the trophozoite is pictured in the problem and has a classic "shield-like" appearance. FA 2019 pg. 155 has more information and the sketchy for it was really good!
Per FA, DOC for giardia = metronidazole. MOA of metronidazole = formation of toxic free radical metabolites in the bacterial cell wall that damage DNA making it bactericidal and antiprotozoal. Metro treats = GET GAP = giardia, entamoeba, trichomonas, Gardnerella, anaerobes (below diaphragm), and H. pylori (as an alternative to amoxicillin in PCN allergy). Adverse effects = disulfiram-like reaction, HA, and metallic taste. I didn't know what Tinidazole is, and found out it is of the same drug class as Metronidazole, so makes sense why it would also be used for Giardia. For the purpose of the UMSLE 1, though, I think metronidazole would be DOC (especially because tinidazole isn't in FA).
This is not in FA btw.
I though in this one as a sick sinus syndrome hahaha in UW.
I think you meant 2(29/30)(1/30) just to clarify!
i am confusion
You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal.
2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1
x x = _ = ____
1 1 30 30 15
Nevermind :/ It didn't come out as planned :(
This patient does not undergo a water deprivation test
Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early.
Just wondering why it in not resistance to ADH action of vasopressin
because he would be hypernatremic with no ADH. can't resorb any water
low osm/urine, low os/plasma => psychogenic polydipsia